The effect of one year's swimming exercise on oxidant stress and antioxidant capacity in aged rats

The effect of exercise on oxidant stress and on alterations in antioxidant defense in elderly has been investigated extensively. However, the impact of regularly performed long-term physical activity starting from adulthood and prolonged up to the old age is not yet clear. We have investigated the changes in the activities of antioxidant enzymes - superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) - and lipid peroxidation in various tissues of rats which had performed (old-trained) or had not performed (old-control) regular swimming exercise for one year. These animals were compared with young-sedentary rats. Increased lipid peroxidation was observed with ageing in all tissues (heart, liver, kidney, striated muscle) and swimming had no additional effect on this elevation of lipid peroxidation. Heart and striated muscle SOD activites, and striated muscle CAT activity increased as a consequence of ageing, whereas kidney and liver CAT activities, as well as GPx activities in kidney, liver, lung and heart were significantly decreased compared to young controls. Lung and heart SOD, liver CAT activities as well as GPx activities in liver, lung and heart were increased significantly in rats which performed exercise during ageing, compared to the old-control group. These findings suggest that lifelong exercise can improve the antioxidant defense in many tissues without constituting any additional oxidant stress.     

Pro-antioxidant ratio in healthy men exposed to muscle-damaging resistance exercise

The purpose of this study was to compare the pro-antioxidant status in healthy men exposed to muscle-damaging resistance exercise, and to investigate the practical application of Loverro's coefficient (P/A ratio) to evaluate the presence of oxidative stress. Twenty-eight healthy men were assigned to two groups performed multi-joint (M) or single-joint (S) resistance exercise. The activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) as well as the concentration of lipid peroxidation products (TBARS) in blood were evaluated. The P/A ratio was calculated from the mean values of erythrocyte TBARS, SOD, CAT and GPx. Creatine kinase (CK) activity was used as a marker of muscle damage. The applied resistance exercises triggered off the changes in pro-antioxidant ratio towards peroxidation which was proved by significant increase in erythrocyte TBARS concentration in M (+25%) and S (+27%) groups. Plasma TBARS increased only after multi-joint resistance exercise and correlated with erythrocyte P/A ratio (r = 0.536, P < 0.01). The multi-joint exercise caused decrease in SOD activity by 28% whereas the single-joint resistance exercise elevated enzyme activity by 20%. Activities of the other antioxidant enzymes changed simultaneously i.e. CAT activity increased by 14%-16% immediately after exercise, and GPx activity declined by 18%-34% during recovery in M and S groups. Even though, all erythrocyte parameters significantly changed following multi-joint and single-joint resistance exercises, the assessment of pro-antioxidant ratio showed the considerable increase in P/A only in M group. In summary, an analysis of pro- and antioxidant parameters showed significant changes in response to muscle-damaging exercise and demonstrated the practical application of P/A ratio to evaluate the risk of oxidative stress in athletes.     

Expression of metallothionein in renal tubules of rats exposed to acute and endurance exercise

The induction of exercise-induced apoptosis in not actively involved in exercise organs, such as kidney could be a result of oxidative stress. Metallothionein (MT) exerts a protective effect in the cell against oxidative stress and apoptosis. We have previously demonstrated an increased incidence of apoptosis in distal tubular cells and collecting ducts in rat kidney after acute exercise. The present study was designed to test the hypothesis that MT may play a protective role in rat renal tubules against exercise-induced apoptosis after the acute exercise and regular training. Male Wistar rats were divided into control, acute exercised and 8-wk regularly trained groups. The kidneys were removed after a rest period of 6 h and 96 h. The ultrastructure of renal tubular cells was examined by electron microscopy. Apoptosis was detected in paraffin sections by the TUNEL technique. Expression of MT was examined by immunohistochemistry. The level of lipid peroxidation (thiobarbituric acid reactive substances - TBARS) was assayed in renal tissue homogenates. After acute exercise, the occurrence of apoptosis was restricted to distal tubules and collecting ducts of rat kidney, whereas the proximal tubules remained unaffected. The 8-wk training did not result in increased apoptosis in tubular cell. MT expression was confined exclusively to proximal tubules in all groups. However, it was significantly increased in acutely exercised animals, as compared to control and trained rats. After the 8-wk training, MT expression remained unaltered as compared to the control group. TBARS levels were significantly increased after acute exercise, while after regular training they remained unchanged. A significant correlation between TBARS level and MT expression was demonstrated. The findings could suggest a protective role of MT against oxidative stress and apoptosis in proximal tubular cells.     

Antioxidant efficacy of black pepper (Piper nigrum L.) and piperine in rats with high fat diet induced oxidative stress

The present study was aimed to explore the effect of black pepper (Piper nigrum L.) on tissue lipid peroxidation, enzymic and non-enzymic antioxidants in rats fed a high-fat diet. Thirty male Wistar rats (95-115 g) were divided into 5 groups. They were fed standard pellet diet, high-fat diet (20% coconut oil, 2% cholesterol and 0.125% bile salts), high-fat diet plus black pepper (0.25 g or 0.5 g/kg body weight), high-fat diet plus piperine (0.02 g/kg body weight) for a period of 10 weeks. Significantly elevated levels of thiobarbituric acid reactive substances (TBARS), conjugated dienes (CD) and significantly lowered activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and reduced glutathione (GSH) in the liver, heart, kidney, intestine and aorta were observed in rats fed the high fat diet as compared to the control rats. Simultaneous supplementation with black pepper or piperine lowered TBARS and CD levels and maintained SOD, CAT, GPx, GST, and GSH levels to near those of control rats. The data indicate that supplementation with black pepper or the active principle of black pepper, piperine, can reduce high-fat diet induced oxidative stress to the cells.     

Thiamine deficiency induces oxidative stress in brain mitochondria of Mus musculus

The present investigation evaluates the changes in the levels of antioxidant enzymes, lipid peroxidation (LPO), and protein carbonyl content (PCC) in brain mitochondria following thiamine deficiency (TD). The study was carried out on Mus musculus allocated into three groups, namely control and thiamine-deficient group for 8 (TD 8) and 10 (TD 10) days. The LPO was measured in terms of reduced glutathione (GSH) and thiobarbituric acid reactive substance (TBARS). Antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were measured biochemically. A significant increase in the TBARS (p?<?0.0001) and PCC (p?<?0.001) levels in group II (TD 8) and group III (TD 10) animals was observed in comparison to controls. The GSH levels were found to be reduced in both the treated groups compared to the control. A significant reduction in the activities of SOD was also observed in group II (p?<?0.01) and group III (p?<?0.0001) animals in comparison to the control. Enzymatic activities of CAT (p?<?0.001) and GPx (p?<?0.05) were found to be significantly reduced in group III (TD 10) in comparison to the control. In conclusion, reduction in the activities of antioxidant enzymes as well as an increase in LPO and PCC following TD implies oxidative stress in brain mitochondria that may further leads to neurodegeneration.     

Effects of Chronic Restraint Stress and 17-β-Estradiol Replacement on Oxidative Stress in the Spinal Cord of Ovariectomized Female Rats

Previous studies have shown sex-specific oxidative changes in spinal cord of rats submitted to chronic stress, which may be due to gonadal hormones. Here, we assessed total radical-trapping potential (TRAP), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities and lipid peroxidation (evaluated by the TBARS test) in the spinal cord of ovariectomized (OVX) female rats. Female rats were subjected to OVX, and half of the animals received estradiol replacement. Animals were subdivided into controls and chronically stressed (for 40 days). Our findings demonstrate that chronic stress decreased TRAP, and increased SOD activity in spinal cord homogenates from ovariectomized female rats and had no effect on GPx activity. On the other hand, groups receiving 17β-estradiol replacement presented a decreased GPx activity, but no alteration in TRAP and in SOD activity. No differences in the TBARS test were found in any of the groups analyzed. In conclusion, our results support the idea that chronic stress induces an imbalance between SOD and GPx activities, additionally decreasing TRAP. Estradiol replacement did not reverse the effects of chronic stress, but induced a decrease in GPx activity. Therefore, estradiol replacement in ovariectomized chronically stressed rats could make the spinal cord more susceptible to oxidative injury.     

Dietary induction of angiotensin-converting enzyme in proximal and distal rat small intestine

Induction of angiotensin-converting enzyme was examined in proximal and distal intestinal segments of rats fed a low-protein (4%) diet and then switched to a high-protein (gelatin) diet. Animals were killed at varying time points, and brush-border membranes and total RNA were prepared from the segments. In the proximal intestine, there was a fivefold increase in angiotensin-converting enzyme levels after 14 days but only a twofold change in mRNA. In the distal intestine, there was no increase in enzyme activity but mRNA increased 2.4-fold. Organ culture was used to measure changes in enzyme biosynthesis. There was a 5- to 6-fold increase in the biosynthesis of angiotensin-converting enzyme in the proximal intestine 24 h after the switch to the gelatin diet and a 1.6-fold increase in mRNA levels. No change in biosynthesis was observed in the distal small intestine despite an increase in mRNA. These results support the conclusion that rapid dietary induction of intestinal angiotensin-converting enzyme is differentially regulated in proximal and distal segments of the small intestine.     

Optimization of selenium status by a single intraperitoneal injection of Se in Se-deficient rat: possible application to burned patient treatment

In order to investigate the efficiency of a single selenium (Se) administration in restoring selenium status, Se and antioxidant enzymes were studied in an animal model of Se depletion. In Se-depleted animals receiving or not a single parenteral administration of Se, plasma, red blood cell (RBC), and tissue Se levels were measured concurrently with glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities. The oxidative stress was assessed by thiobarbituric acid-reactive species (TBARs), total thiol groups, glutathione, and tocopherol measurements. Our study showed that Se depletion with alterations in the antioxidant defense system (Se and GPx activity decreases) led to an increase of lipid peroxidation, a decrease of the plasma vitamin E level, and SOD activation. Sodium selenite injection resulted after 24 h in an optimal plasma Se level and a reactivation of GPx activity. In liver, brain, and kidney, Se levels in injected animals were higher than those in reference animals. However, this single administration of Se failed to decrease free radical damage induced by Se depletion. Therefore, in burned patients who exhibit an altered Se status despite a daily usually restricted Se supplementation, the early administration of a consistent Se amount to improve the GPx activity should be of great interest in preventing the impairment of the antioxidant status.     

Damaging effects of intense repetitive treadmill running on murine intestinal musculature

Several gastrointestinal symptoms associated with prolonged intense exercise (IE) have been reported, although the mechanisms underlying its effects on the intestine remain poorly understood. The aim of the present study was to investigate whether IE may induce oxidative stress in the intestine, as well as its possible relationship with intestinal signaling impairments, leading to contractile disturbances. C57BL/6 mice were submitted to 4 days (EX.4D) and 10 days (EX.10D) of IE. The daily exercise session consisted of a running session until exhaustion, with the treadmill speed set at 85% of each animal's maximum velocity. The decrease in exhaustion time was exponential, and the reduction in the maximum velocity, as assessed by an incremental test, was higher in EX.4D than in EX.10D animals. The ileum mucosa layer was partially destroyed after 4 days of IE, where 37% and 11% muscle layer atrophies were observed in EX.4D and EX.10D animals, respectively. Ileum contractility was significantly impaired in the EX.4D animal group, with reduced efficacy for carbachol, bradykinin, and KCl signaling associated with a decrease in lipid peroxidation and with no alteration of protein oxidation. Intestinal myocytes from EX.10D animals displayed areas containing structurally disorganized mitochondria, which were associated with increased levels of protein oxidation, without alteration of contractility, except for a reduction in the potency of bradykinin signaling. Finally, no clear relationship between ileum contractility and oxidative stress was shown. Together, these results argue in favor of significant functional, biochemical, and morphological disturbances caused by exercise, thus demonstrating that intestinal tissue is very sensitive to exercise.     

Vascular redox imbalance in rats submitted to chronic exercise

Exercise training has been used for treatment/prevention of many cardiovascular diseases, but the mechanisms need to be clarified. Thus, our aim was to compare oxidative stress parameters between rats submitted to a swimming training and sedentary rats (control). Twelve male rats were divided into two groups: control and exercise training. The exercise training had daily 1 h swimming sessions for 8 weeks and a load (5% of its body mass) was placed in rat's tail. Thereafter the animals were killed, aorta and heart were surgically removed and blood was collected. Body mass gain, thiobarbituric acid reactive species (TBARS), carbonyl content, total reactive antioxidant potential (TRAP), total antioxidant reactivity (TAR), superoxide dismutase (SOD) activity and catalase (CAT) activity were evaluted. The trained rats showed a lower body mass gain and no modifications on heart. An increased SOD activity was observed on aorta after the training, but no changes were seen for CAT activity, which led to an increased SOD/CAT ratio. The arterial TBARS was also increased for trained rats. The decrease in TRAP in exercise training was the single modification on plasma. Our findings suggest that the increased SOD activity could play a role in vascular adaptations to exercise training. Copyright © 2010 John Wiley & Sons, Ltd.     

Lipid peroxidation and scavenger enzymes during exercise: adaptive response to training

This study was designed to determine whether endurance training would influence the production of lipid peroxidation (LI-POX) by-products as indicated by malondialdehyde (MDA) at rest and after an acute exercise run. Additionally, the scavenger enzymes catalase (CAT) and superoxide dismutase (SOD) were examined to determine whether changes in LIPOX are associated with alterations in enzyme activity both at rest and after exercise. Male Sprague-Dawley rats (n = 32) were randomly assigned to either trained or sedentary groups and were killed either at rest or after 20 min of treadmill running. The training program increased oxidative capacity 64% in leg muscle. After exercise, the sedentary group demonstrated increased LIPOX levels in liver and white skeletal muscle, whereas the endurance-trained group did not show increases in LIPOX after exercise. CAT activity was higher in both red and white muscle after exercise in the trained animals. Total SOD activity was unaffected by either acute or chronic exercise. These data suggest that endurance training can result in a reduction in LIPOX levels as indicated by MDA during moderate-intensity exercise. It is possible that activation of the enzyme catalase and the increase in respiratory capacity were contributory factors responsible for regulating LIPOX after training during exercise.     

Exercise-induced oxidative stress affects erythrocytes in sedentary rats but not exercise-trained rats.

Oxidant stress is one of the factors proposed to be responsible for damaged erythrocytes observed during and after exercise. The impact of exertional oxidant stress after acute exhaustive treadmill running on erythrocyte damage was investigated in sedentary (Sed) and exercise-trained (ET) rats treated with or without antioxidant vitamins C and E. Exhaustive exercise led to statistically significant increments in the levels of thiobarbituric acid-reactive substance (TBARS) and H2O2-induced TBARS in Sed rats and resulted in functional and structural alterations in erythrocytes (plasma hemoglobin concentrations, methemoglobin levels, and rise in osmotic fragility of erythrocytes with decrease in erythrocyte deformability). Administration of antioxidant vitamin for 1 mo before exhaustive exercises prevented lipid peroxidation (TBARS, H2O2-induced TBARS) in Sed rats without any functional or structural alterations in erythrocytes. Parameters indicating erythrocyte lipid peroxidation and deterioration after exhaustive exercise in rats trained regularly with treadmill running for 1 mo were not different from those in Sed controls. Erythrocyte lipid peroxidation (TBARS) increased in exhausted-ET rats compared with ET controls; however, the plasma hemoglobin, methemoglobin levels, and erythrocyte osmotic fragility and deformability did not differ. Exhaustive exercise-induced lipid peroxidation in ET rats on antioxidant vitamin treatment was prevented, whereas functional and structural parameters of erythrocytes were not different from those of the ET controls. We conclude that exertional oxidant stress contributed to erythrocyte deterioration due to exercise in Sed but not in ET rats.     

Antioxidant effect of eugenol in rat intestine

The effect of eugenol on the antioxidant status of the rat intestine after short and long term (15 days and 90 days respectively) oral administration of 1000 mg/kg.b.wt (a dosage which has been reported to be highly hepatoprotective) was studied. The level of lipid peroxidation products (TBARS) and the activities of glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD) and catalase (CAT) were found to be near normal on eugenol treatment. The level of glutathione (GSH) did not show any change on 15 days of eugenol treatment, but it was increased significantly on 90 day eugenol treatment. The activity of glutathione-S-transferases (GSTs) was increased significantly in both 15 day eugenol treated and 90-day eugenol treated groups. The results suggest that eugenol is nontoxic, protective and induces glutathione-S-transferases (GSTs) and thereby it may facilitate the removal of toxic substances from the intestine.     

Temperature increase results in oxidative stress in goldfish tissues. 2. Antioxidant and associated enzymes

Activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST), glutathione reductase (GR), and glucose-6-phophate dehydrogenase (G6PDH) were measured in four tissues of goldfish, Carassius auratus L., over 1-12 h of high temperature (35 degrees C) exposure followed by 4 or 24 h of lower temperature (21 degrees C) recovery. SOD activity was strongly affected by heat shock, increasing 4-fold in brain, liver, and kidney, but was mainly reversed at recovery. In some tissues, activities of SOD, catalase, GPx, and G6PDH decreased significantly after 1 h heat shock exposure suggesting that thermal inactivation possibly occurred, but were renewed at further exposure. In many cases, 4 h of return to the initial temperature decreased enzyme activities. High correlation coefficients between SOD activities and levels of lipid peroxidation products suggest that these products might be involved in up-regulation of antioxidant defense. Several enzymes (SOD, GST, GR) responded to stress in coordinated manner.     

Ghrelin Acts as an Antioxidant Agent in the Rat Kidney

Ghrelin has recently been shown to improve renal function in rat with acute renal failure. In this setting, the protective effects have been suggested to be due to its antioxidant properties. Thus, the aim of this study was to measure the antioxidant abilities of this hormone via enzymatic and lipid peroxidation analyses. Wistar rats were divided into two control and two treatment groups, the treated animals receiving 3 nmol of ghrelin as subcutaneous administrations on each of 10 consecutive days and physiological saline injected to controls. Catalase (CAT) activity was significantly higher in the treated animals when compared to controls, while in contrast, lipid peroxidation measured by thiobarbituric acid reactive substances (TBARS), was significantly reduced in the ghrelin treated animals. Furthermore, superoxide dismutase (SOD) activity and glutathione (GSH) content were both much higher in treated female rats than in controls and although there was a slight increase in glutathione peroxidase (GPx) activity in kidneys of ghrelin treated rats, the difference was insignificant. These findings suggest that ghrelin has beneficial antioxidant properties in the rat kidney by increasing antioxidant enzyme activities. These effects were more noticeable in treated female rats, possibly due to higher levels of estrogen.     

Cytoprotective effects of carvedilol against oxygen free radical generation in rat liver

The protective effects of carvedilol, an antihypertensive agent, against oxidative injury caused by acetaminophen were studied in rat liver. Male Wistar rats (250 +/- 30 g) were pre-treated with carvedilol (3.6 mg/kg, p.o.) for 10 days and on the 11th day received an overdose of acetaminophen (800 mg/kg, p.o.). Four hours after acetaminophen administration, blood was collected to determine serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT). After that, rats were killed and the livers were excised to determine reduced glutathione (GSH), thiobarbituric acid reactive substances (TBARS) and carbonyl protein contents, and the activity of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione S-transferase (GST), and also the DNA damage index. Acetaminophen significantly increased the levels of TBARS, the DNA damage and SOD, AST and ALT activities. Carvedilol was able to prevent lipid peroxidation, protein carbonilation and DNA fragmentation caused by acetaminophen. Moreover, this drug prevented increases in SOD, AST and ALT activities. These results show that carvedilol exerts cytoprotective effects against oxidative injury caused by acetaminophen in rat liver. These effects are probably related to the O2*- scavenging property of carvedilol or its metabolites.     

Hypoxia and recovery perturb free radical processes and antioxidant potential in common carp (Cyprinus carpio) tissues

The effects of hypoxia exposure and subsequent normoxic recovery on the levels of lipid peroxides (LOOH), thiobarbituric acid reactive substances (TBARS), carbonylproteins, total glutathione levels, and the activities of six antioxidant enzymes were measured in brain, liver, kidney and skeletal muscle of the common carp Cyprinus carpio. Hypoxia exposure (25% of normal oxygen level) for 5h generally decreased the levels of oxidative damage products, but in liver TBARS content were elevated. Hypoxia stimulated increases in the activities of catalase (by 1.7-fold) and glutathione peroxidase (GPx) (by 1.3-fold) in brain supporting the idea that anticipatory preparation takes place in order to deal with the oxidative stress that will occur during reoxygenation. In liver, only GPx activity was reduced under hypoxia and reoxygenation while other enzymes were unaffected. Kidney showed decreased activity of GPx under aerobic recovery but superoxide dismutase (SOD) and catalase responded with sharp increases in activities. Skeletal muscle showed minor changes with a reduction in GPx activity under hypoxia exposure and an increase in SOD activity under recovery. Responses by antioxidant defenses in carp organs appear to include preparatory increases during hypoxia by some antioxidant enzymes in brain but a more direct response to oxidative insult during recovery appears to trigger enzyme responses in kidney and skeletal muscle.     

Temporal variations of lipid peroxidation products, antioxidants and liver marker enzymes in experimental hyperammonemic rats

Circadian variations of lipid peroxidation products: thiobarbituric acid and reactive substances (TBARS), antioxidants: reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and liver marker enzymes such as transaminases (aspartate transaminase (AST) and alanine transaminase (ALT), alkaline phosphatase (ALP) and γ-Glutamyl transpeptidase (GGT) in circulation were analysed in control and ammonium chloride (AC) induced (100 mg/kg bodyweight) hyperammonemic rats. Elevated lipid peroxidation and liver marker enzymes (increased mesor of TBARS, AST, ALT, ALP and GGT) associated with decreased activities of antioxidants (decreased mesor of GPx, GSH, SOD and CAT) were found in hyperammonemic rats. Variations in acrophase, amplitude and r values were also found in between the control and hyperammonemic rats. These alterations clearly indicate that temporal liver marker enzymes and redox status are modulated during hyperammonemic conditions, which may also play a crucial role in disease development.     

Proline Alters Antioxidant Enzyme Defenses and Lipoperoxidation in the Erythrocytes and Plasma of Rats: In Vitro and In Vivo Studies

In the present study, we investigated, in vivo (acute and chronic) and in vitro, the effects of proline on the activities of antioxidant enzymes such as catalase (CAT), glutathione peroxidase and superoxide dismutase (SOD) in erythrocytes and also investigated the effect on thiobarbituric acid-reactive substances (TBARS) in the plasma of rats. For the experiments, the number of animals per group ranged from eight to ten. For acute administration, 29-day-old rats received one subcutaneous injection of proline (18.2 μmol/g body weight) or an equivalent volume of 0.9% saline solution (control) and were killed 1 h later. For chronic treatment, buffered proline was injected subcutaneously into rats twice a day at 10 h intervals from the 6th to the 28th day of age. Rats were killed 12 h after the last injection. For in vitro studies, proline (30.0 μM to 1.0 mM) was added to the incubation medium. Results showed that acute administration of proline reduced CAT and increased SOD activities, while chronic treatment increased the activities of CAT and SOD in erythrocytes and TBARS in the plasma of rats. Furthermore, in vitro studies showed that proline increased TBARS in the plasma (0.5 and 1.0 mM) and CAT activity (1.0 mM) in the erythrocytes of rats. The influence of the antioxidants (α-tocopherol plus ascorbic acid) on the effects elicited by proline was also studied. Treatment with antioxidants for 1 week or from the 6th to the 28th day of age prevented the alterations caused by acute and chronic, respectively, proline administration on the oxidative parameters evaluated. Data indicate that proline alters antioxidant defenses and induces lipid peroxidation in the blood of rats.     

Protective effect of glycine supplementation on the levels of lipid peroxidation and antioxidant enzymes in the erythrocyte of rats with alcohol-induced liver injury

We studied the effect of glycine supplementation on lipid peroxidation and antioxidants in the erythrocyte membrane, plasma and hepatocytes of rats with alcohol-induced hepatotoxicity. Administering ethanol (20%) for 60 days to male Wistar rats resulted in significantly elevated levels of erythrocyte membrane, plasma and hepatocyte thiobarbituric acid reactive substances (TBARS) as compared with those of the experimental control rats. Decreased activities of superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), glutathione peroxidase (GPx) and glutathione reductase (GR) were also observed on alcohol supplementation as compared with those of the experimental control rats. Glycine was administered at a dose of 0.6 g kg(-1) body weight to rats with alcohol-induced liver injury, which significantly decreased the levels of TBARS and significantly elevated the activities of SOD, CAT, GSH, GPx and GR in the erythrocyte membrane, plasma and hepatocytes as compared to that of untreated alcohol supplemented rats. Thus, our data indicate that supplementation with glycine offers protection against free radical-mediated oxidative stress in the erythrocyte membrane, plasma and hepatocytes of animals with alcohol-induced liver injury.